Department of Pediatrics, Kansai Medical University, 10-15 Fumizono-cho, Moriguchi-shi, Osaka 570-8506, Japan
- Mots-clés : glucocorticoid, mRNA, PEPCK
- DOI : 10.1684/mrh.2012.0321
- Page(s) : 131-9
- Année de parution : 2012
Many epidemiological studies have reported the link between magnesium deficiency and metabolic syndrome. We examined whether magnesium deficiency in rats induces changes in glucocorticoid metabolism. Twelve-week-old, female Wistar rats were weaned onto a very low-magnesium diet or a control diet for two weeks. Quantitative real-time PCR was used to assess mRNA for 11β hydroxysteroid dehydrogenase-1 (11β-HSD1), 11β-HSD2, phosphoenolpyruvate carboxykinase (PEPCK), peroxisome proliferator-activated receptor α (PPARα), and glucocorticoid receptor in the liver. Concentrations of adiponectin, leptin, corticosterone, insulin and asymmetric dimethylarginine (ADMA) in fasting serum were determined using a rat-specific enzyme-linked immunosorbent assay. After two weeks, no differences in serum glucose, leptin, corticosterone, or adiponectin levels were observed between the groups. Magnesium-deficient rats showed higher HOMA-IR, insulin, ionized calcium, ADMA levels and diastolic blood pressure. There were no significant differences in hepatic mRNA expression levels of GR, 11β-HSD1, 11β-HSD2, or PPARα between the groups. We observed lower expression of hepatic PEPCK mRNA, in the magnesium-deficient rats, thus suggesting a possible compensatory mechanism to diminish glycogenesis. A low-magnesium diet alters glucocorticoid metabolism, which leads to endothelial damage. Higher ADMA induces hypertension and insulin resistance. Hyperinsulinemia induces hepatic down-regulation of PEPCK, and is possibly a key mechanism inducing the metabolic complications of magnesium deficiency.